05 Postdoctoral Fellowship at Umea University, Sweden 

This postdoc position at the department of informatics is a part of the Wallenberg AI, Autonomous Systems and Software Program on Humanities and Society (WASP-HS), which aims to realize excellent research and develop competence on the consequences and challenges of artificial intelligence and autonomous systems for humanity and society. This 10-year program is initiated and generously funded by the Marianne and Marcus Wallenberg Foundation (MMW) with 660 million SEK. In addition to this, the program receives support from collaborating industry and from participating universities. 

This postdoctoral position is part of a Swedish council financed research project to unravel the regulation of programmed cell death at the molecular level with focus on the structure of the proteins and biological membranes involved in this important process. Important key players in the mitochondrial (intrinsic) cell death pathway are membrane-active proteins of the Bcl-2 family. The main objective of this project is to understand the function – and underlying structural properties – of these proteins and their interactions with the mitochondrial membrane environment. For this purpose we will use structural biological methods focusing on solid-state NMR spectroscopy of lipid-protein complexes, complemented by liquid-state NMR. In addition, we will also use neutron reflectometry on these lipid protein complexes). You will primarily study the membrane bound Bcl-2 proteins and their mutual interactions.  In addition, you will also be supporting NMR based work on human protein kinases which can be involved in human cancer, in part, through their regulation of Bcl-2 proteins.

Inflammation of the gums (gingivitis) is very common and is caused by bacteria found in connection with the teeth and gums. Due to factors that are not fully understood, only some develop periodontitis, which means that the gingivitis process turns into an extensive destruction of the collagen-rich connective tissue and bone that constitute the attachment of the teeth. Bone loss is not only seen in periodontitis, but also in, for example, peri-implantitis and rheumatoid arthritis. In these diseases, bone loss is considered an irreversible condition that risks impairing the function of teeth, implants and joints. However, the molecular mechanisms behind inflammatory bone loss are not fully mapped. Our hypothesis is that there are common molecules that cause inflammation-driven bone loss in individuals who, due to genetic factors, are more susceptible to disease. The overall aim of the project is to identify markers to detect who is at risk of suffering from inflammatory bone loss, such as periodontitis, before the bone breakdown begins. With our research, we also want to discover new osteoimmunological principles that could be attacked with targeted therapy to slow down or prevent inflammation-driven bone loss.

It is not known how stable silencing of alternative gene programs is maintained once a neuronal identity has been established. This project aims to understand fundamental molecular mechanisms underlying maintenance of differentiated serotonergic and dopaminergic neuronal identity and function. Both cell types are involved in several psychiatric disorders which take a huge toll on individuals and society. In addition, midbrain dopamine neurons of the substantia nigra pars compacta constitute the key population whose degeneration is associated with Parkinson’s disease, further underscoring the clinical significance of the project.

Autophagy is an evolutionarily conserved self-eating process mainly purposed to eliminate or recycle dysfunctional cellular organelles or unused proteins. Autophagy plays an important role in development and ageing and has been associated with diverse human diseases including cancer, neurodegeneration and pathogen infection. Autophagy modulation is implicated in the treatment of diseases such as neurodegeneration and cancer.